This study is the first to test PTC sensitivity in a cohort of participants who were originally identified as being at ultra-high risk for psychosis. PTC taster status at follow-up examinations did not discriminate those who later developed psychosis or schizophrenia from those who did not develop psychosis. Furthermore, a family history of either general psychopathology or more specifically psychosis-spectrum disorder was not associated with reduced PTC sensitivity. Therefore, findings in this large UHR cohort do not support previous reports of a higher prevalence of PTC non-tasters among participants with a diagnosis of schizophrenia. Rather, these results suggest that the development of schizophrenia and other psychotic disorders is not associated with PTC taster status.
Our psychophysical protocol was similar to that reported by Compton et al. (2007)
where a comparison strip was administered before presentation of a PTC-containing strip. This protocol was not followed in previous reports, and we reiterate the point that schizophrenia participants are more likely to report that they have tasted something when there is no comparable reference and it remains unclear as to whether the older studies instructed the participants that the PTC paper (or strips) would have an expected bitter taste which further confounds the procedure. In addition, the number of participants with chronic schizophrenia in the Compton et al. (2007)
study were similar in the reports by Moberg et al. (2005
; n = 42): [Compton et al. (2007
; n = 48)] except that 11.5% of the Compton cohort was diagnosed with schizoaffective disorder. Only forty-three percent of the cohort of Moberg et al. (2005)
were tasters of PTC, which was subsequently replicated in a larger independent sample (Moberg et al., 2007
; n = 67, 43%). In contrast, the proportion of PTC tasters in the Compton cohort of schizophrenia participants was considerably higher at 69.6%. Compton et al. (2007)
further suggested that medication status may explain in part the discrepancy of PTC taster status in their subject population when compared to the findings of Moberg et al. (2005
Findings from the current study, albeit from a relatively small number who were diagnosed with schizophrenia (n = 15), suggest that 86.7% (n = 13) could taste PTC during treatment at the PACE clinic. Regarding our larger total cohort, 78 clients (35.6%) reported a family history of psychosis, of whom 69.2% were PTC tasters. This proportion of PTC tasters is similar to that generally reported for healthy Caucasians (Mascie-Taylor et al., 1983
). This finding is also similar to the proportion of first-degree relatives who were tasters in the Compton et al. (2007)
study. Our findings are also consistent with the enhanced methodology employed by Compton et al. (2007)
and, as such, do not support PTC insensitivity as an endophenotypic marker for schizophrenia.
Other factors may influence the disposition of PTC taster status as our cohort ages. For example, potential epigenetic changes such as cytosine methylation in the TAS2R38
gene, or changes in histone modifications, have not been examined. Additional factors may include the methodology used to present PTC, chronicity, or ethnicity of the subject population (Drayna, 2005
). Further research in a large first-episode cohort is warranted, where larger numbers of participants with schizophrenia can be compared to true age-matched controls.
One caveat to the current findings must be noted. It has been reported that psychophysical testing by means of papers or strips impregnated with PTC may lead to a high incidence of false positive responses from insensitive participants (Lawless, 1980
). This finding appears to arise from variability in the procedures employed to accurately classify participant responses as to whether they “taste something.” A more reliable way for future studies to resolve some of the discrepancies is to identify TAS2R38
haplotypes in neuropsychiatric and control populations. Provided that the delivery method for PTC has been successfully validated (GS, submitted), genetic analysis of the PTC receptor would circumvent any procedural differences. This genetic data would directly address, on a genetic level, the question of taster-non-taster status in this clinical population.